Marie-Sylvie Roy

Contrast dependency of VEPs as a function of spatial frequency: the parvocellular and magnocellular contributions to human VEPs

The present study investigated the contrast dependency of visual evoked potentials (VEPs) elicited by phase reversing sine wave gratings of varying spatial frequency. Sixty-five trials were recorded for each of 54 conditions: 6 spatial frequencies (0.8, 1.7, 2.8, 4.0, 8.0 and 16.0 c deg(-1)) each presented at 9 contrast levels (2, 4, 8, 11, 16, 23, 32, 64 and 90%). At the lowest spatial frequency, the waveform contained mainly one peak (P1). For spatial frequencies up to 8 c deg(-1), P1 had a characteristic magnocellular contrast response: it appeared at low contrasts, increased rapidly in amplitude with increasing contrast, and saturated at medium contrasts. With increasing spatial frequency, an additional peak (N1) gradually became the more dominant component of the waveform. N1 had a characteristic parvocellular contrast response: it appeared at medium to high contrasts, increased linearly in amplitude with increasing contrast, and did not appear to saturate. The data suggest the contribution of both magnocellular and parvocellular responses at intermediate spatial frequencies. Only at the lowest and highest spatial frequencies tested did magnocellular and parvocellular responses, respectively, appear to dominate.

Maturation of Binocular Pattern Visual Evoked Potentials in Normal Full-Term and Preterm Infants from 1 to 6 Months of Age

The purpose of this study was to evaluate the visual development of preterm infants from 1 to 6 mo of age, using the pattern visual evoked potentials (VEP) in response to three check sizes: 60, 30, and 15 min of arc. Pattern VEP were recorded in 24 full-term and 24 preterm infants (26–36 wk of gestation). The results showed a rapid visual maturation between 1 and 3 mo, followed by a slower progression over the next 3 mo, in both groups. The implicit time of the P100 wave of the pattern VEP was also found to shorten with increasing check sizes. The maturation of pattern VEP in preterm infants was shown to be related to their gestational (or corrected) age rather than their postnatal age. The pattern VEP obtained in response to a 60-min check size in preterm infants aged between 1.5 and 2.5 mo (corrected age) showed a tendency for a faster maturation than those of full-term infants. Our results suggest that within the first 6 mo of age, pattern VEP response is useful to monitor visual development in full-term infants as well as in preterm infants using corrected age.

Magnocellular and parvocellular developmental course in infants during the first year of life.

The visual system undergoes major modifications during the first year of life. We wanted to examine whether the magnocellular (M) and parvocellular (P) pathways mature at the same rate or if they follow a different developmental course. A previous study carried out in our laboratory had shown that the N1 and P1 components of pattern visual evoked potentials (PVEPs) were preferentially related to the activity of P and M pathways, respectively. In the present study, PVEPs were recorded at Oz in 33 infants aged between 0 and 52 weeks, in response to two spatial frequencies (0.5 and 2.5 c deg−1) presented at four contrast levels (4, 12, 28 and 95%). Results indicate that the P1 component appeared before the N1 component in the periods tested and was unambiguously present at birth. The P1 component showed a rapid gain in amplitude in the following months, to reach a ceiling around 4–6 months. Conversely, the N1 component always appeared later and then gained in amplitude until the end of the first year without reaching a plateau. Latencies were also computed but no developmental dissociation was revealed. Results obtained on amplitude are interpreted as demonstrating a developmental dissociation between the underlying M and P pathways, suggesting that the former is functional earlier and matures faster than the latter during the first year of life

Prevention of postasphyxial increase in lipid peroxides and retinal function deterioration in the newborn pig by inhibition of cyclooxygenase activity and free radical generation

ABSTRACT: Free radicals have been implicated in the development of injury to the immature retina. Asphyxia increases free radicals as well as prostaglandins (PG) in neural tissues. We assessed whether in the retina the cyclooxygenase pathway contributes to free radical formation after oxidative insults such as asphyxia, which in turn disrupts retinal function. Newborn pigs were treated with either saline, ibuprofen (194 μmol/kg i.v.), or allopurinol (1 mmol/kg i.v.), and retinal malondialdehyde (MDA), hydroperoxides, PGE2 and PGF2α levels, and the amplitudes and implicit times of the a- and b-waves of the full-field electroretinogram were measured before and 1 h after a 5-min period of asphyxia. In saline-treated animals, asphyxia caused a marked increase (p < 0.01) in MDA, hydroperoxides, PGE2, and PGF2α concentrations in the retina. This was associated with a significant decrease (p < 0.01) in the b-wave amplitude measured under scotopic and photopic conditions and an increase in the b-wave implicit times. Ibuprofen and another cyclooxygenase inhibitor, indomethacin (28 μmol/kg i.v.), decreased PGE2 and PGF2α levels and prevented the increase in MDA and hydroperoxides after asphyxia. Allopurinol maintained low concentrations of MDA and hydroperoxides after asphyxia. Both ibuprofen and allopurinol prevented the postasphyxial changes in the b-wave amplitude and diminished the delay in implicit time observed after asphyxia in saline-treated pigs. Our findings suggest that in the retina after asphyxia free radicals appear to originate primarily from the cyclooxygenase pathway and contribute to the deterioration in retinal electrophysiologic function of the newborn animal. Cyclooxygenase inhibitors, like free radical scavengers, may protect retinal function from deteriorating after oxidative stresses.

Light Induces Peroxidation in Retina by Activating Prostaglandin G/H Synthase

Prostaglandin G/H synthase (PGHS) has been shown to generate peroxides to a significant extent in the retina and absorbs light at the lower end of the visible spectrum. We postulated that PGHS could be an important initial source of peroxidation in the retina exposed to light, which would in turn alter retinal function. Exposure of pig eyes (in vivo) to light (350 fc/3770 lx) caused after 3 h a 50% increase and by 5 h a 30% decrease in a- and b-wave amplitudes of the electroretinogram (ERG) which were comparable at 380-650 nm and 380-440 nm but were not observed at wavelengths > 450 nm. These effects of light were prevented by free radical scavengers (dimethylthiourea and high-dose allopurinol) and PGHS inhibitors (naproxen and diclofenac), but stable analogs of prostaglandins did not affect the ERG. Both increases and subsequent decreases in ERG wave amplitudes following light exposure in vivo were associated with increases in retinal prostaglandin and malondialdehyde (peroxidation product) levels, which were inhibited by the nonselective PGHS blockers, naproxen and diclofenac. Similar observations were made in vitro on isolated porcine eyecups as well as on retinal membranes exposed to light (250 fc/ 2700 lx) 380-650 nm and 380-440 nm but not at > 500 nm. Both PGHS-1 and PGHS-2 contributed equivalently to light-induced prostaglandin synthesis, as shown after selective PGHS-2 blockers, but mRNA expression of PGHS-1 and 2 was not affected by light. Finally, light stimulated activities of pure PGHS-1 and PGHS-2 isozymes, and these were also shown to produce superoxide radical (detected with fluorogenic spin trap, proxyl fluorescamine). Taken together, data suggest that PGHS- (1 and 2) is activated by short wavelength visible light, and in the retina is an important source of reactive oxygen species which in turn alter retinal electrophysiological function. PGHS thus seems a likely chromophore in setting forth photic-induced retinal injury. Findings provide an explanation for increased sensitivity of the retina to visible light predominantly at the far blue range of its spectrum.

On- and off-responses in the photopic electroretinogram in complete-type congenital stationary night blindness.

We examined the on- and off-responses of the photopic electroretinogram in patients with complete congenital stationary night blindness. Standard flash electroretinograms as well as those produced in a ganzfeld modified for long-duration light stimuli (500 msec) permitted the separation of on- and off-responses in four patients and four normal subjects. The amplitude and latency of the electroretinogram on- response (a- and b-waves) and off-response (d-wave) in addition to the oscillatory potentials of the off-response in normal subjects and patients were compared. The abnormal on-response was demonstrated in all the patients, and the offresponse with its oscillatory potentials were preserved. We showed that the second portion of the off-response (of inner retinal origin) is normal. If congenital stationary night blindness is a defect of depolarizing bipolar cells, these results preclude input of the depolarizing bipolar cells and support the hyperpolarizing bipolar cells as the cellular origin of the off-response electroretinogram.

Developmental delay and magnocellular visual pathway function in very-low-birthweight preterm infants

This study investigated the effect of very preterm birth (gestation ≤30wks) and very low birth weight (≤1500g) on the development of magnocellular and parvocellular visual processing streams. Participants were preterm infants (n=55: 31 females, 24 males) born between 24 and 30 weeks’gestation (mean 27.4wks [SD 1.3]), weighing between 720 and 1470g (mean 1015g [SD 215]) and term infants (n=52: 27 females, 25 males) born between 38 and 42 weeks’gestation (mean 39.4wks [SD 0.9]), weighing between 2670 and 4405g (mean 3549g [SD 440]). Visual‐evoked potentials to phase‐reversing sine‐wave gratings, varying in spatial frequency and contrast, were used to elicit magnocellular and parvocellular specific responses. Previous studies found that the N1 component reflects the parvocellular response, while P1 reflects the magnocellular response in adults and infants. Findings from the current study indicate significantly lower P1 amplitudes in preterm compared with term infants under most conditions. No difference was found for the amplitude of the N1 waveform. Results indicate that, for the age‐range tested, preterm birth has little effect on the development of parvocellular function, while it appears to disrupt the development of magnocelluar function.

Alterations in the Electroretinogram of Newborn Piglets by Propionic Acid–Derivative Nonsteroidal Antiinflammatory Drugs but Not by Indomethacin and Diclofenac

ABSTRACT: Different nonsteroidal antiinflammatory drugs (NSAID), especially ibuprofen, are being considered as an alternative to indomethacin for use in the newborn and as antipyretics for infants. However, some of these NSAID have been shown to cause visual complications. We therefore studied the effects of different NSAID indomethacin 19.6 μ-mol/kg (7 mg/kg), diclofenac 15.7 μmol/kg (5 mg/kg), ibuprofen 48 and 194 μmol/kg (10 and 40 mg/kg), naproxen 79 μ,mol/kg (20 mg/kg), and flurbipro-fen 41 μmol/kg (10 mg/kg) on photopic and scotopic electroretinograms (ERG) and retinal prostaglandin E2, prostaglandin F2α, and 6-keto-prostaglandin F1α levels in piglets 1–5 d old. All NSAID decreased retinal prostaglandin levels, but their effects on the ERG were not identical. Indomethacin and diclofenac did not alter the ERG. In contrast, the propionic acid derivatives ibuprofen (the two doses used), naproxen, and flurbiprofen affected the amplitude as well as the implicit time of the ERG under photopic and scotopic conditions. These changes are suggestive of generalized alterations in the function of rods and cones. Prior inhibition of prostaglandin synthesis by indomethacin did not modify the effects of ibuprofen on the ERG. These findings thus show a dissociation between the effects of NSAID on the ERG and prostaglandin synthesis. Because ERG changes are associated with visual alterations, these effects of propionic acid derivatives should be taken into account before considering their use in infants.

Delayed Early Primary Visual Pathway Development in Premature Infants: High Density Electrophysiological Evidence

In the past decades, multiple studies have been interested in developmental patterns of the visual system in healthy infants. During the first year of life, differential maturational changes have been observed between the Magnocellular (P) and the Parvocellular (P) visual pathways. However, few studies investigated P and M system development in infants born prematurely. The aim of the present study was to characterize P and M system maturational differences between healthy preterm and fullterm infants through a critical period of visual maturation: the first year of life. Using a cross-sectional design, high-density electroencephalogram (EEG) was recorded in 31 healthy preterms and 41 fullterm infants of 3, 6, or 12 months (corrected age for premature babies). Three visual stimulations varying in contrast and spatial frequency were presented to stimulate preferentially the M pathway, the P pathway, or both systems simultaneously during EEG recordings. Results from early visual evoked potentials in response to the stimulation that activates simultaneously both systems revealed longer N1 latencies and smaller P1 amplitudes in preterm infants compared to fullterms. Moreover, preterms showed longer N1 and P1 latencies in response to stimuli assessing the M pathway at 3 months. No differences between preterms and fullterms were found when using the preferential P system stimulation. In order to identify the cerebral generator of each visual response, distributed source analyses were computed in 12-month-old infants using LORETA. Source analysis demonstrated an activation of the parietal dorsal region in fullterm infants, in response to the preferential M pathway, which was not seen in the preterms. Overall, these findings suggest that the Magnocellular pathway development is affected in premature infants. Although our VEP results suggest that premature children overcome, at least partially, the visual developmental delay with time, source analyses reveal abnormal brain activation of the Magnocellular pathway at 12 months of age.

Neurophysiological correlates of auditory and language development: a mismatch negativity study.

During child development, physiological changes occur in the auditory cortex, which are reflected by differences in the electrophysiological signals. This study aimed to examine the age-related changes of the Mismatch Negativity component (MMN) in response to speech and non-speech stimuli in a cross-sectional design. Results revealed distinct patterns of activation according to stimulus type and age. Age-related differences for tone discrimination occurred earlier in childrens development than did the discriminative process for speech sounds. Therefore, networks involved in speech processing are still immature in late childhood and may be more vulnerable to physiological changes.